Can a single "powerless" mitochondrion in the malaria parasite contribute to parasite programmed cell death in the asexual stages?

Mitochondrion. 2013 May;13(3):254-6. doi: 10.1016/j.mito.2012.10.014. Epub 2012 Nov 1.

Abstract

The protozoan pathogens responsible for malaria are from the Plasmodium genus, with Plasmodium falciparum and Plasmodium vivax accounting for almost all clinical infections. With recent estimates of mortality exceeding 800,000 annually, malaria continues to take a terrible toll on lives and the early promises of medicine to eradicate the disease have yet to approach realization, in part due to the spread of drug resistant parasites. Recent reports of artemisinin-resistance have prompted renewed efforts to identify novel therapeutic options, and one such pathway being considered for antimalarial exploit is the parasite's programmed cell death (PCD) pathway. In this mini-review, we will discuss the roles of the plasmodium mitochondria in cell death and as a target of antimalarial compounds, taking into account recent data suggesting that PCD pathways involving the mitochondria may be attractive antimalarial targets.

Publication types

  • Review

MeSH terms

  • Animals
  • Antimalarials / therapeutic use
  • Apoptosis*
  • Artemisinins / therapeutic use
  • Drug Resistance / genetics
  • Humans
  • Lactones / therapeutic use
  • Malaria, Falciparum / drug therapy
  • Malaria, Falciparum / genetics
  • Malaria, Falciparum / metabolism*
  • Malaria, Falciparum / pathology
  • Malaria, Vivax / drug therapy
  • Malaria, Vivax / genetics
  • Malaria, Vivax / metabolism*
  • Malaria, Vivax / pathology
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Plasmodium falciparum / genetics
  • Plasmodium falciparum / metabolism*
  • Plasmodium vivax / genetics
  • Plasmodium vivax / metabolism*

Substances

  • Antimalarials
  • Artemisinins
  • Lactones
  • artemisin